Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-3-30
pubmed:abstractText
Helicobacter pylori has been assigned as a class I carcinogen because of its relation to gastric adenocarcinoma. Chronic H. pylori infection may lead to severe gastritis, glandular atrophy (AT), and intestinal metaplasia (IM). Strains secreting the vacuolating toxin VacA and producing the cytotoxin-associated antigen CagA (type 1 strains), as well as the blood group antigen binding adhesin (BabA) targeting Lewis(b) antigens, have been associated previously with distal gastric adenocarcinoma (M. Gerhard et al., Proc. Natl. Acad. Sci. USA, 96: 12778-12783, 1999) and may therefore also be related to lesions preceding gastric cancer. Antral and corpus biopsies were collected from 451 patients; 151 were H. pylori positive, as determined by PCR. Gastric biopsies were histologically evaluated for activity of gastritis (G0-G3, granulocyte infiltration), chronicity of gastritis (L1-L3, lymphocyte infiltration), and the presence of IM and/or AT according to the Sydney classification. Simultaneously, the presence of bacterial genes encoding virulence and adherence factors (racAs1/s2, cagA, and babA2) was determined by PCR. The presence of cagA+ and vacAs1 (alone or combined) both correlated with activity and chronicity of gastritis (P < 0.05); however, the overall prevalence of these genes was 60 or 72%, respectively, and was thus relatively frequent. The babA2 gene, encoding the adhesin BabA, was detected in 38% of infected patients and was correlated with the activity of gastritis in antrum and corpus (P < 0.005). cagA+/vacAs1+ strains (suggesting the presence of type 1 strains) that were also babA2 positive were detected more frequently in patients with severe histological alterations (such as G3, IM, or AT) compared with subjects without these changes (P < 0.01). cagA+/vacAs1+ strains that were babA2 negative, however, lacked a significant correlation with severe histological changes, activity, or chronicity of gastritis in antrum and corpus. Adherence of H. pylori via BabA appears to be of importance for efficient delivery of VacA and CagA and may play a special role in the pathogenesis of severe histological changes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1903-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11280745-Adhesins, Bacterial, pubmed-meshheading:11280745-Adult, pubmed-meshheading:11280745-Aged, pubmed-meshheading:11280745-Aged, 80 and over, pubmed-meshheading:11280745-Antigens, Bacterial, pubmed-meshheading:11280745-Bacterial Proteins, pubmed-meshheading:11280745-Bacterial Toxins, pubmed-meshheading:11280745-Biopsy, pubmed-meshheading:11280745-Carrier Proteins, pubmed-meshheading:11280745-Chronic Disease, pubmed-meshheading:11280745-Female, pubmed-meshheading:11280745-Gastritis, pubmed-meshheading:11280745-Gastritis, Atrophic, pubmed-meshheading:11280745-Genotype, pubmed-meshheading:11280745-Granulocytes, pubmed-meshheading:11280745-Helicobacter Infections, pubmed-meshheading:11280745-Helicobacter pylori, pubmed-meshheading:11280745-Humans, pubmed-meshheading:11280745-Intestines, pubmed-meshheading:11280745-Lewis Blood-Group System, pubmed-meshheading:11280745-Lymphocytes, pubmed-meshheading:11280745-Male, pubmed-meshheading:11280745-Metaplasia, pubmed-meshheading:11280745-Middle Aged, pubmed-meshheading:11280745-Stomach
pubmed:year
2001
pubmed:articleTitle
Key importance of the Helicobacter pylori adherence factor blood group antigen binding adhesin during chronic gastric inflammation.
pubmed:affiliation
Department of Medicine II and Gastroenterology, Bogenhausen Academic Teaching Hospital, Technical University, Munich, Germany. christian.prinz@lrz.tum.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't